Ank3 E35a-/- mice carry a CRISPR/Cas9 generated deletion of microexon 35a (E35a) of the ankyrin 3, epithelial (Ank3) gene. ANK3 is an adaptor protein that links membrane proteins to the spectrin/actin cytoskeleton. It is best known as a master organizer of the axon initial segment (AIS) and a leading genetic risk factor for neuropsychiatric and neurodevelopmental disorders such as bipolar disorder, intellectual disability, schizophrenia, and autism. E35a is a 27 nucleotide microexon located in a disordered region between the UPA domain and death domain (DD) in a region important for protein-protein interactions. E35a is included in GABAergic neurons and cerebellar neurons but predominantly skipped in cortical glutamatergic excitatory neurons. Interneurons from homozygous Ank3 E35a-/- mice show increased excitability and somatic Ca2+ activity, without disruption in AIS. These mice exhibit motor defects such as hyperactivity, and expanded step length and stance width. They also display social behavior defects such as reduced sniffing duration and rearing frequency which are mainly driven by females. Homozygous Ank3 E35a-/- mice are viable and fertile.

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Ank3 E35a-/- mice carry a deletion of microexon 35a (E35a) of the Ank3 gene. This mouse line may be useful when studying the effect of microexon E35a loss on the onset of neuropsychiatric and neurodevelopmental disorders.